Guerbet Alcohols And Its Derivatives
GUERBET ALCOHOLS
Guerbet alcohols are the beta branched primary alcohols, which are the condensation products of alcohols. This chemistry has made possible the synthesis of regiospecific, beta-branched hydrophobe which introduces high-purity branching into the molecule. The chemistry has resulted in the preparation of many materials that find applications in metal lubrication, plastic mold release, paper processing, and personal care products.
The reaction involves the following steps:
* Oxidation of alcohols to aldehydes
* Aldol condensation after proton extraction
* Dehydration of the aldol product
* Hydogenation of the allylic aldehyde
The reaction is catalyzed in presence of hydrogen transfer catalyst. These include nickel, lead salts, oxides of copper, lead, zinc, chromium, molybdenum, tungsten, manganese and some palladium compounds. At low temperatures of 130-140°C, oxidation process is the rate limiting step. At somewhat higher temperatures 160-180°C, the rate limiting step is the aldol condensation .At higher temperatures, other degradative reactions occur and can become dominant. Cannizaro reaction is the major side reaction described.
Most commonly used raw materials for the preparation of Guerbet alcohols are alcohols of natural origin which are primary, with even numbered, straight carbon chains. Oxo alcohols can also be used, but the reaction rate and conversions are reduced.
Guerbet alcohols are branched, essentially saturated and of high molecular weight, exhibit the following properties Have low irritation potential Are liquid to low temperatures Are low in volatility Are reactive and can be used to make many derivatives Are good lubricants Exhibit very good oxidative stability at elevated temperatures Have excellent color initially and at elevated temperatures Exhibit improved stability over unsaturated products in many applications.
They are prepared by the oxidation of Guerbet alcohols to produce primary carboxylic acids. Oxidative alkali fusion with alkali metal salts dehydrogenates the alcohol and gives excellent yields of carboxylic acids.
Guerbet alcohols as well as acids melt at lower temperatures than linear alcohols containing the same number of carbon atoms. Compared to Guerbet alcohols with the same number of alcohols corresponding Guerbet acids melt at higher temperature.
GUERBET ESTERS
One of the desired effects of introducing Guerbet branching into ester molecules is to extend their liquidity to very low temperatures. With the availability of Guerbet acids and alcohols, branching can be introduced into the alcohol, acid or both.
It is observed that products with the lowest titer carry Guerbet branching in both the acid and the alcohol part of the molecule. The next lowest titer point is obtained when the Guerbet branch is in the acid moiety. Branching in the alcohol part results in the highest titer value. Products derived from linear acids and linear alcohols differ substantially from those derived from linear acids and Guerbet alcohols. Specifically, the former are rock hard solids while the latter are liquids with a snowy precipitate. Introduction of Gurbet branching in to the ester molecule do not alter the solubility of the resulting ester.
GUERBET SULFATES AND ETHER SULFATES
Sulfates and ether sulfates are typical anionic surfactants. One of the salient properties of surfactant is the Kraft point which is a measure of water solubility. It is defined as the temperature in °C at which a 1% dispersion becomes clear under gradual heat. The Kraft point of sulfates rises with increasing molecular weight of the hydropobe or with the addition of propylene oxide to the hydrophobe. The Kraft point decreases with the addition of ethylene oxide. The Kraft point provides another illustration of the differences between the linear and Gurbet based sulfates.
The location of the branch within the hydrophobe has a major effect upon functional properties of anionic surfactants, such as their HLB and emulsifying power. Guerbet based surfactants promote their micellization in the oil phase because of its twin tail structure which require less cosurfactant to make micro emulsions. Guerbet ether sulfates are very efficient emulsifiers for oil and emulsify three to five times more oil than the sulfates made from linear hydrophobes.
Dr. Prashantkumar Kudli Shrinivas has a vast industrial experience of Aroma chemicals,Essential oils,Perfumery and Flavour formulations. He is a permanent member of Indian Institute of Chemical Engineers & NMR Association of India.
Can I Eat Sugar Alcohols On My Low Carb Diet?
Polyols” or sugar alcohols are a number of different
carbohydrates that are neither sugars nor alcohols–and
are commonly used as artificial sweeteners in a range
of products, from ice cream to chewing gum.While these tasty sweeteners appear to be the perfect
solution for both low-carb dieters and low-carb
food producers, recent studies of sugar alcohols
have painted a somewhat different picture.
To begin with, sugar alcohols are not entirely carb-free.
Most studies have indicated that sugar alcohols contain
approximately 1/2 to 1/3 the amount of calories as
sugar–and in the form of carbohydrates.
In addition, studies have shown that sugar alcohols
are absorbed by the small intestine, but the process
is slower and fractured. This affects a rise
in blood sugar, but again is smaller and more gradual
than with sugar–and the rise tends to vary from
person to person.
Sugar alcohols also have a laxative effect on some
consumers. Since they are only partially absorbed,
they bring water into the bowel–and undigested
carbs into the colon, creating gas and bloating
as the carbs are acted on by bacteria.
Over-consumption of sugar alcohols can often
have an adverse effect on low carb dieters,
even when they can digest them properly.
Sugar alcohols can trigger cravings in
low carb dieters, causing them to deviate
from dietary restrictions.
In addition, sugar alcohols can often cause
low carb dieters to choose an unhealthy
diet of sweets, which appear to be carb-free,
over a varied diet that includes essential nutrients.
If you are currently on a low carb diet and want
to mix sugar alcohol products into your diet,
it is very important that you monitor your total
sugar alcohol intake–and keep it at a minimum while
consuming a healthy diet.
One easy way to do this is to determine the total
amount of carbs in sugar alcohol products you are
consuming. You can do this by subtracting the
amount of fat and protein calories per serving
from the total amount of calories per serving.
Simply multiply the grams of protein by four
and the grams of fat by nine. Now subtract
the sum of the two from the total amount of
calories per serving.
Using these figures, you can determine whether
or not carbs are being “hidden” in “carb free”
sugar alcohol products you consume, allowing
you to make a better-informed decision that
fits the prescriptions of your low-carb diet.
The role of work for wives of alcoholics
The evolution of the research and professional literature on wives of alcoholics covers a continuum of theories from a psychoanalytic orientation regarding the psychopathology of wives, to a sociological approach describing the stress encountered while living while an alcoholic, to a focus on family systems and interaction patterns within the alcoholic family. The Disturbed Personality Hypothesis was the first attempt to describe the behaviors of wives of alcoholics. This hypothesis viewed the wife as an inadequate, dependent woman who married an alcoholic to meet her unconscious personality needs[1-4]. The Decompensation Hypothesis added that attempts by the alcoholic to reduce or stop drinking would result in the personality decompensation of the wife [5-7]Jackson[8] expanded the focus from wives of alcoholics to the adjustment of the total family and the stress of living with alcoholism. She posited that the family passes through seven identifiable stages in attempts to cope with an alcoholic member, while the wife’s personality changes to accommodate the drinking of the alcoholic. Jackson and others who expanded on her work[9-12] concluded that the behavior of wives is specific to the external stressful environment of alcoholism rather than a reflection of the wife’s personality inadequacies. More recently, Moos et al.[13] compared spouses of recovered and relapsed alcoholics to community controls, reporting no increased incidence of disturbed personality or dysfunctional behavior among spouses of recovered alcoholics.
Systems theory, as developed by Steinglass and colleagues[14-16], introduced an interactional framework which helped identify the role of alcohol in stabilizing the family and meeting the needs of its members. By examining family processes within the alcoholic system, it was observed that couples responded to the drinking in a manner that has adaptive consequences for the family. Current models of family dysfunction, spearheaded by adult children of alcoholics proponents, combine a sociological and family systems perspective to focus on the generational transmission of alcoholism[17-21].
However, these theories provide researchers and the treatment community with limited empirical data. The literature on alcoholic families, as noted in recent articles[22, 23], is characterized by narrow conceptual frameworks, anecdotal rather than empirical approaches, and small numbers of subjects. In addition, the majority of studies of the alcoholic family have overlooked the potential value of the work role and its effect in family dynamics. This has been particularly true in the case of the wife of the alcoholic who has been described almost exclusively within the domain of the home. Wives’ employment, if considered, was seen by many as one of several transitory coping responses associated with male alcoholism[8, 9, 11, 24). Even Marital Interaction Theory, which examines family processes within the alcoholic family, did not assess the role of work and its impact on family interactions.
Consideration must be given to the role of work when examining the dynamics of alcoholic families. Work is often viewed as an organizer of daily life. Work contributes to one’s sense of self and gives stability and continuity to that sense once it has been established. Work, then, is a central element in achieving and maintaining a sense of personal identity[25]. Work has been recognized within the social science literature as an important source of social support[26]. Employment could be seen as a long-term role, creating new strains as well as new opportunities for support networks. It also is acknowledged that women do not work solely for financial reasons although that is a common motivator[27]. With the current emphasis on self-development and personal growth, many women view their job as a career which offers significant self-fulfillment[28].
Further, the alcoholism literature needs to recognize the changing nature of the American family and how the movement of women into the work world has fundamentally reshaped the nature of family, work, and society. The number of women in the work force increased 173% from 1947 to 1980[29], with women accounting for 45% of civilians in the labor force today[30]. By the turn of the twenty-first century, women are expected to constitute more than three-fifths of new entrants into the labor force[31]. Family structure, interactions, roles, and behaviors have been markedly influenced by the increasing numbers of women who consider work to be a significant factor in their lives.
Therefore, this study attempted to improve understanding of the dynamics of alcoholism in families as well as the effects of dual employment on the interactions of the family. Both direct and indirect measures were utilized to evaluate the effect of husband’s alcoholism on wives’ work performance, as well as wives’ physical and psychological morbidity.
METHOD
Subjects
The data reported here are part of a larger study of 91 men admitted for inpatient alcoholism treatment. Subjects were participants in three residential treatment programs for substance abuse with an average length of stay of 14 days. Husbands ranged in age from 26 to 63 with a mean age of 42 years. Inclusion criteria were being married or cohabitating for at least the past 3 years, having alcoholism as a primary diagnosis, having no severe psychiatric disorder, and being employed full-time. Consecutive admissions who met the study criteria, who agreed to participate, and whose wives agreed to participate became research subjects. Informed consent was given by all respondents. This paper focuses on those 60 wives of alcoholics who were employed. The wives ranged in age from 23 to 62 years with a mean of 40 years, as shown in Table 1. Ninety-five percent of the wives were high school graduates, with 29% having completed college. These women were typically Catholic and White. Most of the wives were married for the first time, with a median length of marriage at 12 years. The mean number of children living at home was just less than 2, with a range from 0 to 8. None of the women reported problems of alcohol or drug dependence, but half identified themselves as children of alcoholics. This figure is extraordinarily high, given that recent surveys found a lifetime prevalence in only 11.5 to 15.7% of American adults[32].
Recent Animal Models of Alcoholism
Animal models on alcohol preference have a long-standing tradition in biomedical research on alcoholism. However, these models allow only limited conclusions regarding alcohol addiction. Therefore, during the past 15 years, researchers have developed new animal models that mimic different aspects of human alcohol addiction, such as craving, relapse, and loss of control over drinking. These models include the reinstatement model, the alcohol deprivation model, and the point-of-no-return model. Some of these models have been pharmacologically validated with anticraving compounds that are used clinically for treating alcoholics. The detailed behavioral characterization of these new models and their pharmacological validation also allow researchers to study the neurochemical and molecular bases of addictive behavior. KEY WORDS: animal model; trend; research; AOD (alcohol or other drug) preference; AODD (AOD use disorder); relapse; AOD craving; AOD abstinence; anti-alcohol-craving agents; A AOD-seeking behavior
Researchers have known since 1940 that some rodents voluntarily consume alcohol in a laboratory setting. [1] One can also assume that voluntary alcohol consumption by rodents and other mammals occurs in the wild, because some mammals, including rodents, occasionally consume large amounts of rotten fruits and exhibit abnormal behavioral patterns that may result from intoxication. Consequently, voluntary alcohol consumption, which is often observed in combination with palatable food or fluid intake, can be considered a part of the normal behavioral repertoire of rodents. These observations position rats and mice as ideal subjects for studying various aspects of human alcohol use, including alcohol reinforcement. [2] One commonly used approach to modeling human alcohol consumption in rodents are alcohol preference studies, in which the animals are given a choice between water and alcohol solutions and the investigators measure the amount consumed of each fluid. In comparison to other behavioral studies (e.g., anxiety tests), data on alcohol consumption levels obtained by such alcohol preference experiments show little variation, even when conducted in different laboratories (Crabbe et al. 1999) and different settings. Moreover, because alcohol reinforcement is mediated by brain structures that have been strongly conserved during evolution (i.e., subcortical structures), rodent studies have an enormous potential for further elucidating the neurobiological basis of alcohol consumption and alcohol reinforcement processes in humans.
This article presents several rodent models that have been used in recent years to study various aspects of alcohol addiction. The article first reviews traditional alcohol preference models and their limitations. It then describes newer models aimed at helping researchers investigate the rodent equivalent of complex human behaviors, such as craving, relapse, and loss of control over drinking. These models have been validated in pharmacological studies and have provided some insight into the neurochemical and cellular changes underlying addictive behaviors.
ALCOHOL PREFERENCE MODELS
As mentioned previously, researchers have conducted numerous alcohol preference studies in which the animals were offered a free choice between water and alcohol solutions of various concentrations. These studies found that when offered low alcohol concentrations (i.e., up to 6 percent weight/volume), which have a “sweet” taste, rats and mice generally drink more alcohol than water. At higher alcohol concentrations, however, at which the taste of the solution usually is aversive to rodents, large differences exist among individuals and among strains in alcohol preference. These observations suggest that animals primarily prefer alcohol because of such factors as taste, rather than because of its stimulatory effect on the central nervous system. Only a few animals exhibit an alcohol preference that results from alcohol’s pharmacological (e.g., reinforcing) effects.
The large variability in alcohol preference among individual animals and strains has allowed researchers to selectively breed rats for differential alcohol preference, generating pairs of animal strains that are characterized by particularly low or high alcohol consumption levels. The best studied pairs of lines were generated in Finland, the United States, and Sardinia. The Finnish model–called Alko Alcohol (AA) and Alko Nonalcohol (ANA) rats–comprises two strains of albino rats that based on their selection or rejection of a 10-percent alcohol solution and water, were selectively bred starting in 1963 (Eriksson 1968). The alcohol-preferring (P) rats, originally bred in Indiana, voluntarily consume 5-8 grams of alcohol per kilogram of body weight per day (g/kg/day), attaining blood alcohol concentrations of 50-200 mg/100 mL, whereas the non-alcohol-preferring rats (NP) consume less than 0.5 g/kg/day alcohol (McBride and Li 1998). The Sardinian alcohol-preferring (sP) rats also have been selectively bred f or high alcohol preference and consumption for more than 20 years (Colombo 1997). These models have been used as a tool for characterizing the behavioral, neurochemical, and molecular correlates of differential voluntary alcohol consumption and preference.
Future Directions in Alcoholism Research
Alcohol affects the process by which genes direct the synthesis of proteins (i.e., expression). Therefore, patterns of gene expression in the presence of alcohol can help scientists identify the specific molecular sites of alcohol’s actions within the brain. New technologies can detect and quantify changes in the expression of thousands of genes simultaneously by scanning microscopic gene arrays applied to glass or silicon chips an inch or so square. However, genes whose activity is altered in the presence of alcohol may either be contributing to alcoholism development or may be reacting to alcohol’s presence. This question can be researched by observing the effects of manipulating the level of specific gene products. One way to accomplish this end is by means of viruses that have been engineered to express a specific gene in infected cells. This technique has been applied successfully in studying addictive behaviors. It is suggested that patterns of gene expression may become a diagnostic tool, with differen t disease states being characterized by distinct expression profiles. KEY WORDS: gene expression; protein synthesis; genome; virus; mRNA; hippocampus; ventral tegmental area; animal model
Polonged or repeated exposure to alcohol can lead to long-term changes in the function of nerve cells (i.e., neurons) within the brain. Researchers believe that these changes underlie certain manifestations of addictive behavior, such as tolerance, withdrawal, and the persistent craving for alcohol that appears to provoke relapse after prolonged abstinence. The molecular mechanisms underlying these long-term neurological changes largely involve specific brain proteins that play various roles in communication among neurons.
Information encoded in a cell’s genetic material directs the synthesis of a given protein. Thus, in whole organisms, the coordinated control of genes determines an individual’s basic structure. Minor variations among genes account for the normal range of inherited differences between individuals in a population. Conversely, major genetic variation may underlie an individual’s vulnerability to disease. At its most basic level, a dormant gene may become active in response to chemical messengers that signal a cell’s increased need for the gene’s particular protein product. The genetic information contained in the DNA is transcribed in the cell’s nucleus into a form that can be interpreted by the protein-synthesizing components of the cell called messenger RNA (mRNA). The process by which a gene changes its activity in directing the synthesis of its specific mRNA and the resulting protein is called expression.
Research indicates that alcohol affects gene expression (Bachtell et al. 1999). Furthermore, the pattern of gene expression in the presence of alcohol provides evidence for scientists to deduce the specific molecular sites of alcohol’s action within the brain (Miles 1995). This article focuses on two new approaches for analyzing gene expression that show potential for use in aspects of alcoholism research.
GENE EXPRESSION
Differential Expression
The differential expression approach detects and quantifies alterations in gene expression by indirectly measuring mRNA levels. Using this approach, Chen and colleagues (1997) studied differential expression in male rats after long-term (14-day) administration of alcohol. The investigators determined the total RNA content of specific brain regions. One significant difference detected in the alcohol-exposed rats was a striking elevation of a specific mRNA in the hippocampus that lasted up to 48 hours after withdrawal from alcohol (Chen et al. 1997). The hippocampus is involved in learning and memory and may play a role in alcohol-induced memory blackouts as well as seizures that often accompany the acute withdrawal syndrome following cessation of heavy drinking. The specific mRNA was determined to play a role in the synthesis of an enzyme crucial to energy metabolism in mitochondria. Mitochondria are structures within cells where most of the cell’s energy is produced. Based on these considerations, the results of the experiment of Chen and colleagues supports the idea that alcohol exposure causes defects in mitochondria that may also play a role in such health consequences as alcohol-induced liver disease.
In a comparison study of human brain tissue obtained post mortem from alcoholics and nonalcoholics, Fan and colleagues (1999) measured levels of different types of mRNA obtained from different brain regions. Levels of a specific mRNA were higher in the nucleus accumbens of alcoholic brains compared with nonalcoholic brains. This differentially expressed mRNA is known to play a role in the final stages of mitochondrial protein synthesis. The nucleus accumbens is a center of motivation and stress response and is implicated in the development of alcoholism. Taken together, these results are consistent with the possibility that alcohol-induced activation of energy metabolism in the nucleus accumbens plays a role in alcoholism development.
Physician recognition and treatment of alcoholism
The morbidity, mortality, property damage and lost productivity attributable to alcoholism and alcohol abuse are enormous. Approximately 10 percent of adults entering a physician’s office are likely to have an alcohol problem. Little information exists about whether physicians’ attitudes, beliefs or other characteristics affect their likelihood of recognizing or treating alcoholism. Linn and Yager surveyed internists, family physicians and psychiatrists associated with a major university hospital regarding clinical experiences in assessing and treating alcohol abuse. Practice characteristics, political and religious beliefs, attitudes toward substance abuse, beliefs about the efficacy of treatment, personal experiences with substance abuse and socioeconomic variables were studied.
All full-time physician faculty in medicine and psychiatry were asked to complete self-report questionnaires. In addition, clinical faculty affiliated with the departments of general internal medicine, family medicine, gastroenterology and psychiatry were sent the same questionnaire. Of the 629 questionnaires sent, 303 were completed and returned.
Respondents had the following characteristics: 91 percent were white, 87 percent were men, 85 percent were married and 39 percent were academically based fulltime faculty. About 50 percent were board-certified in internal medicine, 24 percent in psychiatry and 14 percent in family practice; 12 percent were not board-certified. Nonrespondents were somewhat more likely to have been in full-time community-based practice than in a full-time academic setting.
The physician sample reported wide variation in attention to and treatment of alcoholism. Although most (62 percent) of the physicians reported seeing four or more patients over the previous year whose drinking had seriously interfered with their health, physician involvement with diagnosis, treatment or referral was considerably less. Nearly 30 percent of the sample reported never having diagnosed an alcohol problem in a patient who had not previously been diagnosed by another physician. About one-third neither regularly counseled patients about alcohol problems nor had referred anyone for outpatient rehabilitation. About half (52 percent) had not referred a patient for inpatient treatment of alcoholism during the year prior to the study.
The physicians who reported more diverse experiences diagnosing and treating alcoholism were significantly more likely to be in high-volume, community-based primary care practices and were significantly less likely to be engaged in academic pursuits. A high degree of physician experience with alcoholism correlated with a higher volume of patient care in the previous two weeks. A stronger belief in the efficacy of treating alcoholism, membership in the Republican party and a greater degree of religious beliefs were also associated with breadth of experience in diagnosing and treating alcoholism. Higher levels of physician experience with alcoholism were negatively related to time spent in administrative activities, classroom teaching and research.
Family physicians reported having more diverse experience working with alcoholic patients than board-certified internists or uncertified physicians. Board-certified psychiatrists and subspecialists were significantly less likely to report having such patient experiences. Recognizing and treating alcoholism were unrelated to physicians’ current or previous use of alcohol or marijuana.
The authors believe that teaching hospitals must do more to integrate the diagnosis and treatment of alcoholism into the clinical and academic environments. In addition, the authors suggest that internists, psychiatrists, subspecialists and older physicians need to raise their consciousness about alcoholism and improve their treatment skills. (Western Journal of Medicine, April 1989, vol. 150, p. 468.)
Alcohol Availability and Domestic Violence
According to the distribution of consumption model, increases in per capita alcohol consumption predict increases in the rate of heavy use and alcohol-related health and social consequences (1). Alcohol availability, in mm, is considered a key influence on alcohol sales and consumption (2, 3). Ecological studies of the relationship among alcohol availability, consumption, and consequences have been conducted at various levels of analysis, ranging from city blocks, to municipalities and counties, to states. Few researchers argue that availability alone explains the variation in rates of alcohol-related problems among given geographic units; rather, the issue is whether it adds substantially to the amount of variance in such rates accounted for by sociodemographic variables such as age and gender structure, ethnicity, and socioeconomic status. On the one hand, a number of studies have shown that the physical availability of alcohol, usually measured in terms of outlet density or laws and ordinances governing sales, explains a significant amount of additional variance in alcohol-related problems such as motor vehicle crashes, liver disease, and violence (4-7). In contrast, others have found that alcohol outlet density adds little to the explanatory power of models comprised of sociodemographic variables (8-12).
The social and health costs of alcohol use and abuse in the United States are considerable (13). Interest in access and availability, and the development of strategies to affect these, have arisen in recent years as individual-level programs and intervention tend to have little influence on alcohol use (14, 15). The present study focuses on a presumed consequence of alcohol use not considered in previous ecological studies of alcohol availability–namely, domestic violence. Individual-level analyses, based on clinical and survey research, show that heavy alcohol use is associated with increased spousal abuse (16-19). However, as Leonard observes (18), there exists a general paucity of methodologically sound and conceptually driven research that examines the role of alcohol in domestic violence, and we know of no other macrolevel analysis that examines this relationship.
In this study, we examine the relationship among sociodemographic factors, alcohol availability (measured in terms of outlet density), and domestic violence. Specifically, we test whether alcohol outlet density adds significantly to a sociodemographic model to explain variation in rates of domestic violence across the 223 largest municipalities in the state of New Jersey. The sociodemographic variables included in the model have been shown in previous research to be associated with higher rates of domestic and other forms of family violence (20-22). These variables include age, family, ethnic and gender composition, poverty level, and population movement. Conceptually, they are derived from social disorganization theory, with the hypothesis that communities that are more socially disorganized will exhibit higher rates of domestic violence, just as they display higher rates of other social problems such as violent crime and child neglect (20, 23, 24).
METHODS
Data were collected for the 223 municipalities in the state of New Jersey with populations greater than 10,000 in the year 1990. The largest municipality in the sample had a population of 275,221 and the smallest a population of 10,074. The mean population size across the 223 municipalities was 27,931 (SD 29,057). Means and standard deviations of study variables are shown in Table 1 and are described below.
Table 1. Means and Standard Deviations for Sociodemographic Variables, Alcohol Availability, and Domestic Violence Rates for the 223 New Jersey Municipalities
Variable Mean SD
Age, family, and gender composition
< 11 years (%) 15.3 2.8
12-17 years (%) 7.3 1.5
18-30 years (%) 18.2 4.8
> 50 years (%) 28.2 7.3
Children per 100 adults 21.1 5.0
Males per 100 females aged 21-64 95.7 5.3
Female-headed households (%) 4.5 3.2
Educational attainment (%)
< High school education 14.1 6.7
University graduates 18.5 9.6
Ethnic composition (%)
Black 9.0 14.6
Latino 6.8 10.6
Poverty
Unemployed (%) 5.1 2.4
Public assistance (%) 4.3 3.6
Median household income ($) 45,646 13,383
Population movement (%)
Current household < 10 years 21.1 4.5
Moved between 1985 and 1990 15.7 4.1
Moved between 1989 and 1990 5.5 2.2
Urbanicity
Population density (per square mile) 4,515 5,270
Alcohol availability
Total outlets per 10,000 population 12.3 8.1
Domestic violence rate (per 10,000 population)
1990 63.5 52.8
1991 70.7 57.9
1992 64.3 54.0
1993 84.7 68.5
1994 92.0 74.7
1995 112.2 91.7
Mean 1990-1995 81.2 63.7
How To Melt Those Belly Fat Without The Crunches
Tired of carrying those extra weights around your middle? Here are some tips that can help you quickly lose weight and inches off that potbelly of yours. There are ways to have a flatter stomach without doing those dreaded crunches.
Belly Fat Busting Tip #1
Increase your protein and decrease your carbohydrates. It can deliver a one-two punch right to the belly. Carbohydrates increase your insulin level which can slow down your metabolism. The body can only metabolize just so much carbohydrates at once that tend to convert the rest to sugar and turned into body fat.
You just need to have 3-4 oz of lean protein with every meal. This kicks your metabolism up a few notches and an extra help of vegetables in order to add more fiber can keep thinks move along nicely. This is the first step to quick weight loss around your belly.
Belly Fat Busting Tip #2
Reduce your alcohol consumption. Alcohol provides no nutrients and each gram of it contains 7 calories. 100% of the calories you consume through alcohols are stored as fat meaning every beverage you consume is converted to fat usually around the belly.
Cutting back to just one or two drinks a couple of times a week will pay huge dividends to your belly fat busting account.
Belly Fat Busting Tip #3
When it comes to junk-food… pick two and you’re through! It means to pick one salty junk food item and one sweet junk food item to keep in your house. Give yourself only one meal per week during which you will eat a small amount of your chosen salty snack food and one meal per week for your sweet snack food.
An example for a salty junk food is having a plain nacho chips with fat-free refried beans, 1oz of reduced-fat, grated cheddar cheese, 4oz of boneless, skinless chicken breast strips seasoned with packaged taco seasoning, some shredded lettuce, and all the Salsa for dinner once a week. And for the sweet junk food is having a large pancake and syrup during Saturday mornings. This will play a major role in busting your belly fat and trimming inches from your waistline.
Belly Fat Busting Tip #4
Another way to bust belly fat is exercise but it doesn’t mean to do those dreaded crunches or go work out at the gym. You can do a structured exercise such as walking on a treadmill, going to an aerobics class for half hour to 45 minutes three times a week. Or you could give yourself a couple of projects to do around the house every week such as cleaning the garage, hand-wash the car, or do some work in the yard. Just schedule 1-2 of these kinds of physical projects every week shortly after eating a meal rich in catabolic/fat burning foods, and your results could far out-strip that working out down at the gym.
Carbohydrates - Why Low Carb and No Carb Diets Don’t Work for Most Women
In our diet and weight conscious culture, carbohydrates are often considered the biggest culprit and even a curse against losing excess weight-thus the plethora of no carb or low carb diets.
Here’s a very simplified description of what happens when you eat carbohydrates: Our pancreas secretes the hormone insulin which controls blood sugar. During digestion, carbs are broken down to the simplest sugar-glucose. How much glucose stays in the blood and how much goes into the cells is regulated by insulin. Our blood sugar levels can shift erratically when insulin levels are too high or too low. Diabetes is the consequence of high blood sugar levels (hyperglycemia). Headaches, spaciness, shakiness, muscle weakness and mental confusion are some of the symptoms of low blood sugar (hypoglycemia).
Carbohydrates convert to glucose and our brains need glucose to function optimally. In my opinion a no carb and sometimes even low carb diet is asking for BIG trouble. Women especially need balanced portions of healthy carbs to produce serotonin-the brain chemical mastering moods, controlling cravings, satiety (fullness), sex drive, and sleep. If our serotonin levels are too low, we may experience depression, anxiety, irritability, difficulty sleeping and cravings for carbs, chocolate, tobacco or alcohol. (Anti-depressants just help us keep what serotonin we already have, they don’t produce it-thus the dependency.)
Self-medication: When our bodies are not producing enough of the ‘happier mood’ chemicals and hormones, we often ’self-medicate’ with mood enhancer imposters like refined carbs (sweets, desserts, processed foods, chips etc) tobacco, alcohol or drugs which make us feel better temporarily. Our body is tricked by these imposters so it stops producing the happier mood chemicals. Since the imposters are not produced naturally, the cycle of addiction begins and we continually need our food or drug fix in order to feel happier.
We can choose to eat more complex rather than refined carbohydrates: Complex carbs take longer for the body to digest and don’t usually spike our blood sugar. Brown rice, whole grains, sprouted grains, whole fruits, beans and legumes are complex carbohydrates. Processed foods and snacks, desserts, juices, pop and sugars are refined carbohydrates. Fruits are natural simple carbs. Most refined and some simple carbs can spike our blood sugar dramatically. High Fructose Corn Syrup(HFCS) is the BIGGEST culprit in spiking blood sugar and added to many food products. I invite you to read about the havoc HFCS wreaks in our body online and to be sure to read labels on all foods before purchasing.
One way to avoid ’spiking’ is to eat some protein with carbs to slow down the whammy to our blood sugar. When we eat a small amount of protein with carbs assimilation slows down and becomes more balanced.
An exception is melons (watermelon, cantaloupe, honeydew etc) Since melon sugars are broken down rapidly, if combined with protein (which takes much longer to digest) the sugars will stay in the stomach too long and become fermented and can cause digestive issues. To avoid this, always eat melons by themselves at least 20-30 minutes before other foods.
Insulin Resistance: Since blood sugar is an issue for a lot of people-including me, I am beginning to learn about insulin resistance (IR). IR is a condition where insulin is blocked from carrying glucose into the cells so the pancreas pumps out more insulin to overcome the resistance. In Chapter 6 of her book The Feel Good Diet Dr. Cheryl Hart states that at least of 75% of overweight Americans have some degree of insulin resistance. Uncontrolled insulin resistance can lead to high blood pressure, fat around the waist, diabetes, heart attacks and strokes. The Feel Good Diet is easy to read, very educational and offers lots of recipes to lose weight and keep blood sugar levels normal. Dr. Hart has a quiz in her book to determine if you are insulin resistant. Dr. Hart offers 1-Day clinics to educate women about natural hormone replacement and weight loss. I attended both clinics and came away feeling confident about listening to the signals my body sends when something is ‘off kilter’ and learning what I can do to bring myself back to balance. While I don’t agree with all of the foods she recommends in her recipes, most of her information is terrific.
Some guidelines when insulin resistant: Always eat protein with a carb (1/2 cup or 4 ounces of carbohydrate to 1 ounce of protein) Eat low fat, not no fat. Most vegetables are insulin neutral. These fruits are not insulin spiking if eaten raw and may be eaten without protein: apples, apricots, cherries, peaches, pears, plums, nectarines, grapefruit, lemons and limes.
A few examples of carb/protein balancing:
# Unsweetened yogurt or cottage cheese (protein) with fresh fruit (carb)
# Chocolate candy with nuts (protein) and dark chocolate rather than milk chocolate
# Almond or peanut butter (protein) spread on bread (carb)
# Milk (protein) with cereal carb)
# Egg or cheese with toast
Artificial Sweeteners: I HIGHLY RECOMMEND AVOIDING ALL artificial sweeteners-Equal, Splenda, Sugar Twin and Sweet n’ Low. You can check out the health dangers online.
Healthier Natural Sweeteners: Many of us like to sweeten our coffee, tea, oatmeal, cold cereal or hot cereal. Healthier alternatives to refined white sugar are Stevia, Organic Blue Agave Syrup (my favorite), honey, maple syrup, rice syrup, raw sugar and organic sugar. The first two are lower in the Glycemic Index scale. Some people find Stevia has a bitter aftertaste. If you’re not familiar with the Glycemic Index you can find information online.
Some natural sweetener substitutes may cause excess gas, bloating and digestive distress-sorbitol, malitol and zylitol are the most common of the sugar alcohols. Erythritol is least likely to cause digestive disturbances and has zero calories and is zero on the Glycemic Index and has not been found to affect blood sugar or insulin levels.
Only you can know how many carbohydrates you need to eat in your daily diet. If you have any questions, please be sure to check with your health professional.
Essential Tips For Proper Food Combining
As any student of chemistry will assure you, acids and bases (alkalis) neutralize each other. If you eat a starch with a protein, digestion is impaired or completely arrested! The undigested food mass can cause various kinds of digestive disorders. Undigested food becomes soil for bacteria, which ferment and decompose it. Its by products are poisonous, one of which, alcohol, is a narcotic that destroys or inhibits nerve function. It plays havoc with nerves of the digestive tract, suspending their vital action such that constipation may well be a result! These are the salient rules for proper food combining.
The Basic Rules of Proper Food Combining:
1. Eat acids and starches at separate meals. Acids neutralize the alkaline medium required for starch digestion and the result is fermentation and indigestion.
2. Eat protein foods and carbohydrate foods at separate meals. Protein foods require an acid medium for digestion.
3. Eat but one kind of protein food at a meal.
4. Eat proteins and acid foods at separate meals. The acids of acid foods inhibit the secretion of the digestive acids required for protein digestion. Undigested protein putrefies in bacterial decomposition and produces some potent poisons.
5. Eat fats and proteins at separate meals. Some foods, especially nuts, are over 50% fat and require hours for digestion.
6. Eat sugars (fruits) and proteins at separate meals.
7. Eat sugars (fruits) and starchy foods at separate meals. Fruits undergo no digestion in the stomach and are held up if eaten with foods that require digestion in the stomach.
8. Eat melons alone. They combine with almost no other food.
9. Desert the desserts. Eaten on top of meals they lie heavy on the stomach, requiring no digestion there, and ferment. Bacteria turn them into alcohols and vinegars and acetic acids.